Assessment of neuroprotective effects of Gallic acid against glutamate-induced neurotoxicity in primary rat cortex neuronal culture

• Published in: Neurochemistry international Vol. 121; pp. 50 - 58
• Main Authors: Maya, S., Prakash, T., Madhu, Krishnadas
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.12.2018
• Subjects: Gallic acid; Glutamate excitotoxicity; Neurodegenerative diseases; Neuronal protection; Neurotoxicity; sALS; NO; Neuronal protection; HRP; GLU; Neurotoxicity; MAP2; CSF; NMDA; GA; GSH; Glutamate excitotoxicity; PBS; Gallic acid; Neurodegenerative diseases; DTNB; TMB; IGF; SOD; EDTA; NAA; NOS; ROS; RCN; GAPDH
• ISSN: 0197-0186; 1872-9754; 1872-9754
• DOI: 10.1016/j.neuint.2018.10.011

Glutamate excitotoxicity plays a crucial role in the pathogenesis behind the development and progression of several neurodegenerative diseases. The study aimed to investigate the neuroprotective activity of Gallic acid (GA) against glutamate-induced neurotoxicity in primary rat cortex neurons (RCN). Treated the RCNs with GA 25 & 50 μg/ml for 2 h and later treated the cells with 100 μM glutamate (GLU) and incubated for 24 h at 37 °C. The results demonstrated that, the GA improved the antioxidant profile in the cortex neurons and inhibited the production of the proinflammatory cytokine. GA also maintained the Ca2+ homeostasis, IGF-1 expression, and protected the neurons from glutamate-induced neuronal toxicity. The neuroprotective activity of GA has further confirmed from the results of N-acetylaspartate and expression of microtubule-associated protein-2 expression. The reports suggest that, GA is significantly attenuated the glutamate-induced neurotoxicity and protected neurons from various chemical events that are involved in the pathogenesis of neurotoxicity. •Glutamate excitotoxicity is a major pathogenesis behind the development and progression of neurodegenerative diseases.•Glutamate-induced neurotoxicity in RCN is mediated through the formation of free radicles and proinflammatory cytokine.•Glutamate treatment also caused an alteration in Ca2+ homeostasis and decline in IGF-1 level.•Observed a down-regulation of MAP-2 expression and NAA concentration in glutamate treated rat cortex neurons.•Treatment with GA improved the antioxidant status in neurons and inhibited proinflammatory cytokine production.•GA also maintained the Ca2+ homeostasis, IGF-1 expression, and protected neurons from glutamate-induced neuronal toxicity.